Українська English

ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2014; 60(6): 27-35


S.V. Chorna, N.A. Strutynska, O.M. Semenykhina, S.O. Talanov, V.E. Dosenko, A.V. Kotsuruba, G.L. Vavilova, V.F. Sagach

    Bogomoletz Institute of physiology NAS of Ukraine, Kyiv, Ukraine


The effect of long exercise training on the indexes of the functional state isolated by Lanhendorf heart of old rats during ischemia-reperfusion, the sensitivity of calciuminduced mitochondrial permeability transition pore (MPTP) opening and the role of NO-dependent mechanisms of poreformation regulatory were investigated. Thus, reperfusion injury of the heart contractile function and its myocardial oxygen metabolism were less pronounced in old rats adapted to exercise long training pointing for its positive effect. It is shown a decreased sensitivity of MPTP to its inductor Ca2+ in the heart of old trained rats due to an increase by 1.5-2 orders in threshold Ca2+ concentration, which induces swelling of organelles. At the same time, in heart mitochondria of trained adult rats we observed almost doubled activity of constitutive NO-synthase (cNOS) compared with control (6,02 Ѓ} 0,08 and 3,64 Ѓ} 0,27 pmol / min * mg protein, respectively (P.0,05 )) and a slight increase in the activity of inducible NO-synthase (iNOS). Regulation of pore formation in older animals trained was performed by a significant decreased iNOS activity compared with control aged rats (12,29 Ѓ} 3,11 and 9,25 Ѓ} 1,24 pmol/min*mg protein, respectively (P.0,05)) on the background slight increased in cNOS activity. We hypothesized that a decrease in sensitivity of the MPTP-opening occurred due to an increased production of NO pointing to its role as an inhibitor of pore formation during exercise. It has been shown to increase the sensitivity of MPTP to Ca2+ in the heart under the conditions of reduce the NO production by a single injection of NO syhnthase inhibitor N(omega)-nitro- L-arginine methyl ester (L-NAME) in dose of 10 mg/kg to trained animals of all ages. Using real-time polymerase chain reaction we showed that the gene expression of eNOS in the heart was significantly greater than that of nNOS and iNOS. Thus, in the heart of adult trained rats the expression of mRNA nNOS were increased 5 times, mRNA iNOS - 24 times (P <0,05), and the gene expression of eNOS decreased 3.5 times compared with untrained rats. In the heart of old trained rats the expression of nNOS mRNA decreased 4 times (P<0,05) and iNOS mRNA - 2 times compared with the old untrained animals. In heart of old trained rats we observed a workout recovery of eNOS mRNA expression to the values of control adult animals. Taken together, our data suggest that a longterm exercise training improves functional state of the heart during aging and increases the resistance of body to oxidative stress under reperfusion injury due to a decreased sensitivity of MPTP to Ca2+ and increased activity of mitochondrial cNOS.

Keywords: exercise training, heart, ischemia-reperfusion,mitochondrial permeability transition pore, nitric oxide, geneexpression, aging rats.


  1. Hull SS, Vanoli E, Adamson PB Verrier RL, Foreman RD, Schwartz PJ. Exercise training confers anticipatory protection from sudden death during acute myocardial ischemia. Circulation. 1994; 89: 548-552. CrossRef PubMed
  3. Powers, SK, Demirel HA, Vincent HK Coombes JS, Naito H, Hamilton KL, Shanely AR, Jessup J. Exercise training improves myocardial tolerance to in vivo ischemia- reperfusion in the rat. Am J Physiol. 1998; 275: 1468-1477. CrossRef  
  4. Campos JC, Gomes K MS, Ferreira JCB. Impact of exercise training on redox signaling in cardiovascular diseases. Food and Chemic Toxicol. 2013; 62: 107–119. CrossRef PubMed
  6. Williams MA, Fleg JL, Ades PA, Chaitman BR, Miller NH, Mohiuddin SM, Ockene IS, Taylor CB, Wenger NK. Secondary prevention of coronary heart disease inthe elderly (with emphasis on patients ? 75 years of age): An American Heart Association Scientific Statementfrom the Council on Clinical Cardiology Subcommittee on Exercise, Cardiac Rehabilitation, and Prevention.Circulatio. 2002; 105(14): 1735-1743. CrossRef  
  7. Lennon SL, Quindry JC, French JP, Kim S, Mehta JL, Powers SK Exercise and myocardial tolerance to ischaemiareperfusion. Acta Physiol Scand. 2004; 182: 161-169 CrossRef PubMed
  9. Demirel HA, Powers SK, Zergeroglu MA, Shanely R A, Hamilton K, Coombes J, Naito H. Short-term exercise improves myocardial tolerance to in vivo ischemia-reperfusion in the rat. J Appl Physiol. 2001; 91: 2205–2212. CrossRef PubMed
  11. Ciminelli M, Ascah A, Bourduas K, Burelle Y. Short term training attenuates opening of the mitochondrial permeability transition pore without affecting myocardial function following ischemia-reperfusion. Mol Cell Biochem. 2006; 291: 39-47. CrossRef PubMed
  13. Bernardi P, Di Lisa F The mitochondrial permeabilitytransition pore: Molecular nature and role as a target in cardioprotection. J Mol and Cell Cardiol.
  15. Brookes PS. Mitochondrial nitric oxide synthase. Mitochondrion.2004; 3: 187–204. CrossRef PubMed
  17. Lacza Z, Pankotai E, Busija DW. Mitochondrial nitric oxide synthase: current concepts and controversies. Front Biosci. 2009; 14: 4436-4443. CrossRef  
  18. Li H, Forstermann U. Nitric oxide in the pathogenesis of vascular disease. J Pathol. 2000; 90: 244-254 CrossRef  
  19. Chorna SV, Talanov SO, Strutynska NA. Vavilova G.L., Kotsuruba A.V., Gaidai N.M., Sagach V.F. The functional state the rat heart during ischemia-reperfusion, the sensitivity of calcium-induced mitochondrial permeability transition pore opening and the uncoupling protein 3 expression following long exercise training. Fiziol Zh.2010; 56 (2): 13-21.
  21. Sagach VF, Vavilova GL, Rudyk OV, Strutynska NA. Release of unidentified substances of mitochondrial origin--evidence of mitochondrial permeability transition pore opening in the heart mitochondria of rats. Fiziol Zh.2003; 49 (5): 3-12.
  23. Sagach VF, Rudyk OV, Vavilova GL Kotsiuruba AV, Tkachenko JuP. Melatonin recovers ischemic tolerance and decreases the sensitivity of mitochondrial permeability transition pore opening in the heart of aging rats. Fiziol Zh. 2006; 52 (3): 3-14.

© National Academy of Sciences of Ukraine, Bogomoletz Institute of Physiology, 2014-2024.